secondary glaucoma

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Secondary Glaucoma By Jini P. Abraham

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Page 1: Secondary glaucoma

Secondary Glaucoma

ByJini P. Abraham

Page 2: Secondary glaucoma

Definition Glaucoma - Group of disorders characterized by a

progressive optic neuropathy resulting in characteristic appearance of optic disc and a specific pattern of irreversible visual field defects associated with raised intraocular pressure.

Secondary Glaucoma – Group of disorders in which the raised IOP is associated with a primary ocular or systemic disease.

Page 3: Secondary glaucoma

Classification Depending on the mechanism of rise in IOP –

Secondary open angle glaucoma Secondary angle closure glaucoma

Depending on the causative primary disease – Lens - induced glaucoma Inflammatory glaucoma Pigmentary glaucoma Neovascular glaucoma

Page 4: Secondary glaucoma

Classification Glaucomas associated with irido – corneal

endothelial syndromes Pseudoexfoliative glaucoma Glaucomas associated with intraocular

haemorrhage Steroid-induced glaucoma Traumatic glaucoma Glaucoma-in-aphakia Glaucoma associated with intraocular tumours Ciliary block glaucoma

Page 5: Secondary glaucoma

Lens – induced glaucoma Raised IOP secondary to a disorder of crystalline lens

Lens induced

glaucoma

Lens induced secondary angle

closure glaucoma

Phacomorphic glaucoma

Phacotopic glaucoma

Lens induced secondary open angle glaucoma

Phacolytic glaucoma

Lens particle glaucoma

Phacoanaphylactic glaucoma

Page 6: Secondary glaucoma

Phacomorphic glaucoma

Causes - Intumescent lensAnterior subluxation or dislocation of the lens

and spherophakia Pathogenesis – Swollen lens pushes iris forwards,

obliterating the angle Presentation – Acute congestive glaucoma and

shows features of acute primary angle closure glaucoma

Page 7: Secondary glaucoma

Phacomorphic glaucoma Treatment –

Medical treatment – Control of IOP by iv mannitol, systemic acetazolamide and topical beta blockers

Laser iridotomy Cataract extraction

with implantation of PCIOL

Page 8: Secondary glaucoma

Phacolytic glaucoma Trabecular meshwork is clogged by the lens

proteins, macrophages which phagocytose the lens protein and inflammatory debris

Deep anterior chamber and aqueous may contain fine white protein particles, which settle down as pseudohypopyon

Treatment includes medical therapy to lower IOP followed by extraction of hypermature cataractous lens with PCIOL implantation

Page 9: Secondary glaucoma

Lens particle glaucoma Trabecular meshwork is blocked by the lens particles

floating in aqueous humour. Symptoms of acute rise in IOP associated with lens

particles in the anterior chamber Medical therapy to lower IOP and irrigation –

aspiration of the lens particles from the anterior chamber

Page 10: Secondary glaucoma

Phacoantigenic glaucoma

Fulminating acute inflammatory reaction due to antigen – antibody reaction

Granulomatous inflammation in the involved eye Preceding disruption of lens capsule by

extracapsular cataract extraction, penetrating injury of leak of proteins from the capsule

IOP is raised due to inflammatory reaction of the uveal tissue excited by the lens matter.

Page 11: Secondary glaucoma

Phacoantigenic glaucoma

Management includes medical therapy to lower IOP, treatment of iridocyclitis with steroids and cycloplegics and irrigation – aspiration of lens matter from anterior chamber ( if required).

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Glaucomas due to uveitis

Non specific inflammatory glaucoma

Open – angle inflammatory glaucoma

Angle – closure inflammatory glaucoma

Specific hypertensive uveitis syndrome

Fuchs’ uveitis syndrome

Glaucomatocyclitic crisis

Page 13: Secondary glaucoma

Open – angle inflammatory glaucoma

Acute open – angle inflammatory glaucoma

Chronic open – angle inflammatory glaucoma

Mechanism of rise in IOP

Trabecular clogging , trabecular oedema and prostaglandin – induced rise in IOP

Chronic trabeculitis and trabecular scarring

Clinical featuresFeatures of acute iridocyclitis associated with raised IOP with open-angle of anterior chamber

Raised IOP, open angle, no active inflammation but signs of previous episode of uveitis present

Management

Treatment of iridocyclitis and medical therapy to lower IOP by use of hyperosmotic agents, acetazolamide and beta – blockers eye drops

Medical therapyTrabeculectomyCyclodestructive procedures

Page 14: Secondary glaucoma

Angle - closure inflammatory glaucoma

Mechanism of rise in IOP – Secondary angle – closure with pupil block Secondary angle – closure without pupil block

Clinical features – Raised IOP, seclusio papillae, shallow anterior chamber

Management – Prophylaxis – Local steroids and atropine to

prevent formation of synechiae Curative treatment – Medical therapy, surgical or

laser iridotomy and filtration surgery

Page 15: Secondary glaucoma

Pigmentary glaucoma Clogging up of trabecular meshwork

by the pigment particles Patients with Pigment Dispersion

Syndrome Pigment release caused by mechanical

rubbing of the posterior pigment layer of iris with zonular fibrils

Clinical features – Young myopic males Glaucomatous features similar to POAG Deposition of pigment granules in the anterior segment

Page 16: Secondary glaucoma

Pigmentary glaucoma Gonioscopy – pigment

accumulation along the Schwalbe’s line especially inferiorly (Sampaolesi’s line)

Iris transillumination – radial slit – like transillumination defects in the periphery

Treatment is exactly on the lines of POAG

Page 17: Secondary glaucoma

Neovascular glaucoma Intractable glaucoma results due to formation of

neovascular membrane involving the angle of anterior chamber

Etiology – Neovascularization of iris following retinal ischaemia, feature of Proliferative diabetic retinopathy Central retinal vein occlusion Sickle – cell retinopathy Rare causes (intraocular tumours and long

standing retinal detachment)

Page 18: Secondary glaucoma

Neovascular glaucoma Clinical profile –

Pre – glaucomatous stage Open – angle glaucoma stage Secondary angle closure

glaucoma Treatment –

Panretinal photocoagulation Medical therapy not

effective Artificial filtration shunt

(Seton operation)

Page 19: Secondary glaucoma

Glaucoma associated with iridocorneal endothelial (ICE)

syndromes

3 entities – Progressive iris atrophy Chandler’s syndrome Cogan – Reese syndrome

Presence of abnormal corneal endothelial cells which proliferate to form an endothelial membrane in the angle of anterior chamber

Page 20: Secondary glaucoma

Glaucoma associated with iridocorneal endothelial (ICE) syndromes

Clinical features – Affects middle – aged women Progressive iris atrophy – iris features predominates with

corectopia, atrophy and hole formation Chandler’s syndrome – Mild iris changes and corneal

oedema predominates Cogan – Reese syndrome – nodular and diffuse pigmented

lesions of iris, may or may not be associated with corneal changes

Treatment – Medical treatment Trabeculectomy Artificial filtration

Page 21: Secondary glaucoma

Pseudoexfoliative glaucoma

Deposition of an amorphous grey dandruff – like material on the pupillary border, posterior surface of iris and ciliary processes

Associated with secondary open – angle glaucoma Trabecular blockage by the exfoliative material Managed on the same lines as POAG

Page 22: Secondary glaucoma

Glaucoma associated with intraocular haemorrhage

Hyphaema and vitreous haemorrhage Red cell glaucoma – Associated with fresh traumatic hyphaema;

caused by blockage of trabeculae by RBCs in patients with massive hyphaema; associated with pupil block

Haemolytic glaucoma – Clogging of trabecular meshwork by macrophages laden with lysed RBC debris

Ghost cell glaucoma – Aphakic or pseudophakic eyes with vitreous haemorrhage

Hemosiderotic glaucoma – Sclerotic changes in trabecular meshwork caused by iron from phagocytosed hemoglobin

Page 23: Secondary glaucoma

Steroid – induced glaucoma Type of secondary open – angle glaucoma which develops

following topical or systemic steroid therapy Etiopathogenesis –

Glycosaminoglycans (GAG) theory Endothelial cell theory Prostaglandin theory

Symptoms similar to POAG Prevented by judicious use of steroids and regular

monitoring of IOP Treatment –

Discontinuation of steroids Medical therapy by 0.5% timolol maleate Filtration surgery

Page 24: Secondary glaucoma

Traumatic glaucoma Mechanisms –

Inflammatory glaucoma due to iridocyclitis Glaucoma due to intraocular haemorrhage Lens – induced glaucoma due to swollen

lens Angle – closure glaucoma due to anterior

synechiae Epithelial or fibrous growth Angle recession (cleavage) glaucoma

Management – Medical therapy with topical 0.5% timolol and oral acetazolamide and surgical intervention according to situation

Page 25: Secondary glaucoma

Glaucoma – in - aphakia Raised IOP with deep anterior chamber in early

postoperative period Secondary angle – closure glaucoma due to flat

anterior chamber Secondary angle – closure glaucoma due to pupil

block Undiagnosed pre – existing primary open – angle

glaucoma Steroid – induced glaucoma Epithelial ingrowth Malignant glaucoma

Page 26: Secondary glaucoma

Glaucoma associated with intraocular tumours

Malignant melanoma, retinoblastoma Mechanisms –

Trabecular block due to blockage by tumour cells Neovascularization of the angle Venous stasis Angle closure due to forward displacement of iris – lens

diaphragm Treatment – Enucleation of the eyeball

Page 27: Secondary glaucoma

Ciliary block glaucoma Rare condition occurring as

complication of any intraocular operation

Patients with primary angle – closure glaucoma operated for peripheral iridectomy or trabeculectomy

Markedly raised IOP associated with shallow or absent anterior chamber

Clinical features includes severe pain and blurring of vision following any intraocular operation

Page 28: Secondary glaucoma

Ciliary block glaucoma On examination,

Persistent flat anterior chamber Markedly raised IOP Unresponsiveness or even aggravation by

miotics Phakic, aphakic or pseudophakic

Treatment – Medical therapy – 1% atropine drops,

acetazolamide, 0.5% timolol maleate eye drops and iv mannitol

YAG laser hyaloidotomy Surgical therapy

Page 29: Secondary glaucoma

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